ArticleScientific reports2016
Antigen-affinity controls pre-germinal center B cell selection by promoting Mcl-1 induction through BAFF receptor signaling.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 12 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
12 citing papers in PubMed.
- B cell-activating factor modulates the factor VIII immune response in hemophilia A.The Journal of clinical investigation · 2021Trial
- Causal Effects of Immune Cells on Reproductive Ill-Health, Including Abnormal Spermatozoa, Polycystic Ovary Syndrome and Spontaneous Abortion: Mendelian Randomization Analyses.Journal of multidisciplinary healthcare · 2025Article
- Genes Co-Expressed withInternational journal of molecular sciences · 2024Article
- Early B cell transcriptomic markers of measles-specific humoral immunity following a 3Frontiers in immunology · 2024Article
- A BAFFlingHaematologica · 2022Article
- Prolactin promotes proliferation of germinal center B cells, formation of plasma cells, and elevated levels of IgG3 anti-dsDNA autoantibodies.Frontiers in immunology · 2022Article
- Physiological Functions of Mcl-1: Insights From Genetic Mouse Models.Frontiers in cell and developmental biology · 2021Review
- The TNFSF Members APRIL and BAFF and Their Receptors TACI, BCMA, and BAFFR in Oncology, With a Special Focus in Breast Cancer.Frontiers in oncology · 2020Article
- Article
- Hyperactivated PI3Kδ promotes self and commensal reactivity at the expense of optimal humoral immunity.Nature immunology · 2018Article
- Role and Regulation of Pro-survival BCL-2 Proteins in Multiple Myeloma.Frontiers in oncology · 2018Review
- Altered B cell signalling in autoimmunity.Nature reviews. Immunology · 2017Review
Corrections and comments
- Erratum issued
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Upon antigen encounter, the responsive B cell pool undergoes stringent selection which eliminates cells with low B cell receptor (BCR) affinity. Already before formation of the germinal center, activated B cells of low-affinity are negatively selected in a process that is molecularly not well understood. In this study, we investigated the mechanism behind pre-GC affinity-mediated B cell selection. We applied affinity mutants of HEL antigen and found that rapidly after activation B cells become highly dependent on the cytokine BAFF. Moreover, expression of BAFF receptor CD268 is regulated in a BCR-affinity dependent fashion. High affinity responses via BAFF correlated with PI3K activation, which controlled expression of the pro-survival protein Mcl-1, and thereby increased survival. In the presence of excess BAFF, or in absence of the Mcl-1 antagonist Noxa, more low-affinity B cells survived the first two days after antigen encounter. This resulted in increased numbers of antigen-specific B cells of low affinity upon immunization and reduced the overall affinity of cells that contributed to the germinal center reaction. Our findings elucidate a crucial molecular pathway of B cell selection in the earliest phases of activation by identifying a novel link between BCR affinity and BAFF-R signaling towards Mcl-1.
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